Volume 179 - Issue 10
Troponin testing: an audit in three metropolitan hospitals
Author: Richard X Davey
Med J Aust 2003; 179 (10): 558-559. || doi: 10.5694/j.1326-5377.2003.tb05693.x
Published online: 17 November 2003
Published online: 17 November 2003
Richard X Davey
Chemical Pathologist, Melbourne Health Shared Pathology Service, Western Hospital, Footscray, VIC 3011. Richard.DaveyATwh.org.au
In reply: In acute myocardial infarction (AMI) diagnosis, the sensitivity and specificity of troponin rise with time after symptom onset. The sensitivity of troponin-I testing was shown to increase from 35% at 0–4 hours to 97% at 12–24 hours after an infarct.1 Similarly, a meta-analysis found that “multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity” for AMI diagnosis.2 This position is taken by the National Academy of Clinical Biochemistry3 and European and American cardiologists.4
Furthermore, the diagnostic clock starts from a patient’s emergency department presentation if there is any unreliability suspected in the patient’s assessment of pain onset. Pain onset may have been stuttering, indeterminate, simply forgotten, some combination of these, or even absent. Bailey describes several situations such as these, thought to justify, or to explain, singlicate troponin testing, and suggests that, as I did not audit records, I was not able to quantify the true extent of inappropriate ordering. I acknowledged this shortcoming, but believe it does not detract from the endpoint found.
The Bankstown low-risk patients5 are only a confounder here. In our protocol they probably would not have been thought to have cardiac pain, and all the remaining Bankstown patients had serial biomarker testing.
In my audit,6 93% of singlicate troponin test orders did not diagnose an AMI, and if AMI were still considered, then the tests contravened the protocols.3,4 This is why they were called “inappropriate” — no arbitrary whim.
I assumed, moreover, that no clinician ordered a troponin test unless seeking a cause for chest pain. Our protocol begins with chest pain, recognises uncertainty, and leads through to treating an AMI or reconsidering the diagnosis.
Obliquely invoking Ockham’s principle is also dangerous here. Illnesses such as sepsis may “provoke” an AMI, but this must then be investigated independently, and according to its own rules of engagement, which do not alter solely because of the primary (co-)morbidity.
In short, we did know what is appropriate troponin use, and surveyed it. Like Bailey, we look forward to seeing further evidence.
References
- Chiu A, Chan W-K, Cheng S-H, et al. Troponin-I, myoglobin, and mass concentration of creatine kinase-MB in acute myocardial infarction. Q J Med 1999; 92: 711-718. CACGCGEF
- Balk EM, Ioannidis JP, Salem D, et al. Accuracy of biomarkers to diagnose acute cardiac ischemia in the emergency department: a meta-analysis. Ann Emerg Med 2001; 37: 478-494. i1082832
- Wu AHB, Apple FS, Warshaw MM, editors. Recommendations for the use of cardiac markers in coronary artery disease. Washington: AACC Press, 1999. i1082834
- The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined — a consensus document of the joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction. JACC 2000; 36: 959-969. i1082836
- Boufous S, Kelleher PW, Pain CH, et al. Impact of a chest-pain guideline on clinical decision-making. Med J Aust 2003; 178: 375-380. <eMJA full text>
- Davey RX. Troponin testing: an audit in three metropolitan hospitals. Med J Aust 2003; 179: 81-83. <eMJA full text>